{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shi Q"],"funding":["American Heart Association","National Heart, Lung and Blood Institute","BLRD VA","NHLBI NIH HHS","VA","Department of Veterans Affairs"],"pagination":["596-611"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11074799"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(6)"],"pubmed_abstract":["Aims
A mechanistic link between depression and risk of arrhythmias could be attributed to altered catecholamine metabolism in the heart. Monoamine oxidase-A (MAO-A), a key enzyme involved in catecholamine metabolism and longstanding antidepressant target, is highly expressed in the myocardium. The present study aimed to elucidate the functional significance and underlying mechanisms of cardiac MAO-A in arrhythmogenesis.Methods and results
Analysis of the TriNetX database revealed that depressed patients treated with MAO inhibitors had a lower risk of arrhythmias compared with those treated with selective serotonin reuptake inhibitors. This effect was phenocopied in mice with cardiomyocyte-specific MAO-A deficiency (cMAO-Adef), which showed a significant reduction in both in"],"journal":["Cardiovascular research"],"pubmed_title":["Cardiac monoamine oxidase-A inhibition protects against catecholamine-induced ventricular arrhythmias via enhanced diastolic calcium control."],"pmcid":["PMC11074799"],"funding_grant_id":["I01 BX002334","R01 HL157741","20SFRN35200003","R01 HL157781","R01 HL167087","CDA935054","I01-BX002334","R01 HL122863","R01 HL130346","R21 HL057006","R21 HL075006"],"pubmed_authors":["Shih JC","Streeter J","Anderson EJ","Shi Q","Abel ED","Crawford RM","Huo R","Malik H","Hall D","Wang J","Chen B","Song LS"],"additional_accession":[]},"is_claimable":false,"name":"Cardiac monoamine oxidase-A inhibition protects against catecholamine-induced ventricular arrhythmias via enhanced diastolic calcium control.","description":"Aims
A mechanistic link between depression and risk of arrhythmias could be attributed to altered catecholamine metabolism in the heart. Monoamine oxidase-A (MAO-A), a key enzyme involved in catecholamine metabolism and longstanding antidepressant target, is highly expressed in the myocardium. The present study aimed to elucidate the functional significance and underlying mechanisms of cardiac MAO-A in arrhythmogenesis.Methods and results
Analysis of the TriNetX database revealed that depressed patients treated with MAO inhibitors had a lower risk of arrhythmias compared with those treated with selective serotonin reuptake inhibitors. This effect was phenocopied in mice with cardiomyocyte-specific MAO-A deficiency (cMAO-Adef), which showed a significant reduction in both in","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-07T03:25:21.131Z","creation":"2025-04-04T02:54:16.045Z"},"accession":"S-EPMC11074799","cross_references":{"pubmed":["38198753"],"doi":["10.1093/cvr/cvae012"]}}